Journal
AUTOPHAGY
Volume 17, Issue 10, Pages 3260-3261Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/15548627.2021.1953848
Keywords
Autophagy interactome; cellular senescence; inflammation; oxidative stress; proteostasis; regulated protein stability; selective autophagy; stress support networks
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Funding
- Suh Kyungbae Foundation [SUHF-17020068]
- National Research Foundation of Korea [NRF-2019R1C1C1006386, NRF-2020R1A5A1018081, 2020R1I1A1A01072779]
- National Research Foundation of Korea [2020R1I1A1A01072779] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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Autophagy plays a dual role in maintaining cellular homeostasis and promoting cellular senescence, with selective autophagy coordinating stress support networks in senescent cells. Targeting selective autophagy may provide new therapeutic strategies for disrupting the homeostatic state of senescent cells.
Macroautophagy/autophagy is a sophisticated quality control program that limits cellular damage and maintains homeostasis, being an essential part of several lifespan-promoting interventions. However, autophagy is also necessary for full establishment of cellular senescence, a causal factor for many age-related diseases and aging. What lies ahead of us to unravel such a paradoxical role of autophagy in senescence is to identify specific targets degraded by autophagy during senescence and determine their importance in the senescence regulatory network. Recently, we developed the Selective autophagy substrates Identification Platform (SIP) to advance these goals, providing a rich set of autophagy substrate proteins involved in senescence. Our study demonstrated that selective autophagy coordinates the stress support networks in senescent cells by degrading multiple regulatory components, echoing its homeostatic roles in normal cells. Targeting this type of selective autophagy might provide a unique opportunity to develop non-senescence addiction-based therapeutic strategies for senotherapy by disturbing the homeostatic state of senescent cells.
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